Hypertension occurs with greater frequency in the diabetic than in the non-diabetic population. The hypertensive diabetic, usually with evidence of nephropathy, is said to possess a suppressed renin system, although the mechanism for this has not been established. In studying the hypertensive diabetic with low-renin hypertension (LRH), we propose to further characterize the renin-angotensin-mineralocorticoid system by answering the following questions: 1. How often is LRH observed in the hypertensive diabetic with and without complications of neuropathy and nephropathy and is there a parallel decrease in aldosterone production? This question is easily answered by classifying the patients into renin subgroups, by the use of furosemide stimulation or sodium restriction. Plasma aldosterone levels will be measured by radioimmunoassay concurrently. 2. Is there evidence of excess mineralocorticoid production? Radioimmunoassay of plasma 11-deoxycorticosterone (DOC), aldosterone, and cortisol will be performed, under baseline condition, after saline suppression, and after ACTH stimulation. Total plasma mineralcorticoid activity will be measured by a radioreceptor assay using rat kidney mineralocorticoid receptors. 3. Can the preponderance of big renin be responsible for the low-renin state? Big renin is inactive at pH 7.4 but is activated at pH 3.3. A discrepancy between renin before and after acidification and reassay at pH 7.4 points to the presence of big renin. 4. Is there a reduction in renal prostaglandins, which are intimately involved in renin production? Urinary prostaglandin E, known to reflect renal prostaglandin production, will be measured by radioimmunoassay in collaboration with Dr. P.J. Mulrow.